{"id":1518,"date":"2026-05-21T09:23:03","date_gmt":"2026-05-21T09:23:03","guid":{"rendered":"https:\/\/one-peptides.com\/?page_id=1518"},"modified":"2026-10-03T11:32:28","modified_gmt":"2026-10-03T11:32:28","slug":"sarms-what-are-they-how-do-they-work-and-what-does-science-say","status":"publish","type":"page","link":"https:\/\/one-peptides.com\/es\/sarms-what-are-they-how-do-they-work-and-what-does-science-say\/","title":{"rendered":"SARMs \u2014 what are they, how do they work, and what does science say?"},"content":{"rendered":"

Imagine a lock that only fits one type of key. Testosterone – a natural androgen – is the universal key: it opens doors in the muscles, bones, prostate, liver, skin and brain simultaneously. Effect? Muscles grow, bones thicken – but at the same time the prostate enlarges, the skin produces excess sebum, and the liver works under increased load. For decades, scientists have looked for a way to separate these effects: preserving muscle growth and bone density while eliminating unwanted effects on other tissues. The answer – at least theoretically – was SARMs: selective androgen receptor modulators.<\/span>
\nThe following article is educational in nature and is a review of published scientific literature. The studies described were performed in animal models or in vitro, unless otherwise noted. This does not constitute medical advice.<\/span><\/p>\n

What SARMs are \u2014 and what they definitely aren’t<\/span><\/h2>\n

SARM stands for Selective Androgen Receptor Modulator – a selective androgen receptor modulator. The name says a lot: these compounds bind to the androgen receptor (AR), but they do it in a selective way – they activate it in some tissues (skeletal muscles, bones), and in others (prostate, sebaceous glands, liver) they show minimal or no activity.<\/span>
\nThe concept is not new. The pharmaceutical industry began searching for selective AR modulators in the 1990s, motivated by specific clinical needs. <\/strong>Cancer patients lost muscle mass (cachexia). Older adults experienced sarcopenia, a progressive age-related muscle wasting. Osteoporosis caused fractures of vertebrae and femoral necks. Traditional androgen therapy (testosterone, nandrolone) affected muscle and bone mass – but carried with it a whole baggage of androgenic effects.<\/span>
\nSARMs were supposed to be the answer: anabolism without androgenization. Muscles and bones – yes. Prostate, baldness, acne – no. At least that was the hypothesis.<\/strong><\/span>
\nWhat are SARMs not? They are not dietary supplements. They are not approved drugs for human use (no SARMs have received full FDA or EMA registration as of the date of publication of this article). They are not anabolic steroids – although they affect the same receptor. Formally, these are research chemicals that are the subject of ongoing preclinical and clinical research.<\/span><\/p>\n

How do SARMs work at the molecular level<\/span><\/h2>\n

The androgen receptor is an intracellular protein that, after binding to androgen (e.g. testosterone or dihydrotestosterone), translocates to the cell nucleus and affects gene expression. It is this mechanism that is responsible for the development of male characteristics, muscle growth and bone mineralization.<\/span>
\nAnabolic steroids activate the androgen receptor in all tissues indiscriminately<\/strong> \u2014 hence their wide spectrum of effects, both desirable and undesirable. SARMs, on the other hand, after binding to the receptor, cause a conformational change (shape) of the AR protein, which is different from that caused by testosterone. This different conformation recruits different coactivators and corepressors – proteins that determine which genes will be “turned on” in a given tissue.<\/span>
\nThe best analogy is a TV remote with programmable buttons. Testosterone is a universal remote control – you press one button and all channels turn on at the same time. SARM is a remote control in which you have programmed only selected channels: muscles (channel 1), bones (channel 2) – and the prostate (channel 7) and sebaceous glands (channel 12) are turned off.<\/span>
\nIn practice, selectivity is not binary (all or nothing). It’s more of a spectrum. Each SARM has a different selectivity profile – some show stronger anabolic activity in muscle, others in bone, and none is 100% devoid of androgenic activity in “unwanted” tissues. Hence the term “selective”, not “specific”.<\/span><\/p>\n

Generations of SARMs – from the laboratory to clinical trials<\/span><\/h2>\n

The history of SARMs is one of gradual approach to the clinic – although none of them made it to the registration mark.<\/span>
\nFirst generation (1990s) <\/strong>\u2014 non-steroidal compounds developed by pharmaceutical companies: Ligand Pharmaceuticals, GTx Inc., Merck. They were characterized by oral bioavailability (unlike most steroids, which require injection) and a promising selectivity profile in animal models.<\/span>
\nSecond generation (2000-2010) – compounds that entered clinical trials on humans:<\/span><\/p>\n